Conjugated bilirubin in neonates with glucose-6-phosphate dehydrogenase deficiency
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Cited by (58)
Glucose-6-phosphate dehydrogenase deficiency and susceptibility to childhood diseases in Kilifi, Kenya
2020, Blood AdvancesCitation Excerpt :Although all cases in our current study were safely managed in our well-resourced facility, our findings suggest that both historically and in less well-resourced facilities or in the community today, G6PD c.202 deficiency could be a significant cause of long-term neurological damage due to neonatal hyperbilirubinemia.28 Our data support the conclusion made by others29 that G6PD c.202 deficiency does not cause neonatal jaundice through a mechanism that predominantly involves hemolysis. Although mean Hb concentrations were significantly lower in homo/hemizygous-deficient than in wild-type homo/hemizygous wild-type neonates, the difference was small (138 g/L vs 146 g/L) and the prevalence of neither anemia nor severe anemia was significantly increased.
Mutations and Polymorphisms of Genes Active in the Formation and Elimination of Bilirubin With the Potential for Modulating Neonatal Hyperbilirubinemia
2017, Fetal and Neonatal Physiology, 2-Volume SetThe Preterm Infant. A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency
2016, Clinics in PerinatologyCitation Excerpt :G6PD-deficient neonates frequently develop a more moderate form of hyperbilirubinemia, in the main responsive to phototherapy, but sometimes requiring exchange transfusion. The pathophysiology of this hyperbilirubinemia includes a combination of increased hemolysis12 and a predilection for diminished bilirubin conjugation,13 the result, at least in part, of an interaction with a (TA)7 promoter polymorphism of the uridine diphosphate (UDP)-glucuronosyltransferase 1A1 gene (UGT1A1*28) associated with Gilbert syndrome.14 Premature infants are at higher risk for neonatal hyperbilirubinemia and its consequent neurotoxic complications than that for term infants.
Neonatal hemolysis and risk of bilirubin-induced neurologic dysfunction
2015, Seminars in Fetal and Neonatal MedicineCitation Excerpt :In addition, infections also have been implicated in the pathogenesis of this acute hemolysis [29]. Having an impaired ability to conjugate (and hence eliminate) bilirubin also contributes to the development of hyperbilirubinemia [31]. The hepatic enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1) is responsible for conjugating bilirubin to mono- and diglucuronides prior to excretion into the bile.
Glucose-6-phosphate dehydrogenase deficiency and severe neonatal hyperbilirubinemia: a complexity of interactions between genes and environment
2010, Seminars in Fetal and Neonatal MedicineCitation Excerpt :The principle behind this methodology is that small quantities of conjugated bilirubin fractions efflux from the hepatocyte to the serum, and serum determinations of these fractions reflect intrahepatocytic conjugated bilirubin, reflective of bilirubin conjugation.41 Lower serum diconjugated bilirubin fractions were demonstrated in hyperbilirubinemic (STB ≥ 256 μmol/L [15 mg/dL]) G6PD-deficient neonates, compared with G6PD-adequate controls with similar STB values.42 Furthermore, diminished serum total and conjugated bilirubin fractions were found in G6PD-deficient neonates who subsequently developed hyperbilirubinemia compared with those in whom STB remained <256 μmol/L (15 mg/dL).43
Supported in part by the General Research Fund of the Shaare Zedek Medical Center.